Research Paper Volume 16, Issue 8 pp 7174—7187
Promoter hypomethylated PDZK1 acts as a tumorigenic gene in glioma by interacting with AKT1
Figure 5. PDZK1 binds to AKT1 and maintains its phosphorylation. (A) BioGRID (version 3.5) software was used to screen for potential proteins that interact with PDZK1, and AKT1 was found to be a possible binding partner of PDZK1. (B) The “Scansite” (version 4.0) website was utilized to screen for potential proteins that interact with PDZK1, and AKT1 was also found to be a possible binding partner of PDZK1. (C) AKT1 expression data were obtained from the GEPIA datasets; GBM tissues had higher AKT1 expression levels than normal brain tissues. (D) Glioma patients with high AKT1 expression had poor survival. The Kaplan–Meier method was used for this analysis. (E) U251 cells were transfected with Flag-PDZK1. Coimmunoprecipitation showed the interaction between PDZK1 and endogenous AKT1 in U251 cells. (F) The protein expression of AKT1, p-AKT1, mTOR, p-mTOR and GAPDH was detected by Western blotting. PDZK1 knockdown significantly decreased the levels of phosphorylated AKT1 and mTOR proteins.